Diagnosis is confirmed by examination of peripheral blood smears every 8 to 24 hours. The CSF is examined to exclude other possible causes of symptoms in patients with suspected cerebral malaria. Antimalarial chemotherapy, consisting of intravenous quinine or quinidine (in an intensive care unit [ICU] setting) or artesunate, plus doxycycline, tetracycline, or clindamycin, is started without awaiting laboratory confirmation of the clinical diagnosis. Untreated cerebral malaria is generally fatal. Neurologic sequelae are common in survivors and may include motor, sensory, cognitive, or language deficits and seizures.
AFRICAN TRYPANOSOMIASIS
African trypanosomiasis in humans (“sleeping sickness”) is transmitted by infected tsetse flies and takes two forms; in each, a meningoencephalitis may develop. An initial inflammatory skin lesion or chancre may occur a few days after a bite by the infected fly. Infection by T. brucei gambiense (in West and Central Africa) may otherwise be asymptomatic for months or years. Presentation with fever, headache, arthralgia, lymphadenopathy, and hepatosplenomegaly is followed in late stages by neurologic involvement, with lethargy, headache, personality changes, poor concentration, tremor, unsteadiness, and daytime somnolence. With further progression, the patient becomes obtunded; worsening coma leads to death. Infection by T. brucei rhodesiense (in East Africa) leads to a similar but more acute disorder.
Diagnosis requires identification of the trypanosome, typically in a blood smear. The CSF must be examined to confirm the diagnosis and stage the disease. A pleocytosis or increased protein concentration, or both, indicate neurologic involvement; immunoglobulin M (IgM) levels may be increased, and trypanosomes may be present. Serologic tests for the West but not East African disease are available; polymerase chain reaction (PCR) is investigational. Treatment regimens with antiprotozoal agents depend on the offending organism and whether neurologic involvement has occurred.

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